these treatment related myelodysplasia (t-MDS) or leukaemias (t-AL) exhibit variable phenotypes: CMML or RAEB±T in MDS cases, AML most often (M4 or M5a mainly, M1, M2, M5b at times, ALL (and biphenotypic leukaemias), often CD19+; t(4;11) cases are frequently ALL cases.

11q23 rearrangements in treatment related leukaemias were thought to be found mainly following a treatment with anti-topoisomerase II (epipodophyllotoxins) or with an intercalating topoisomerase II inhibitor (anthracyclins), as for some 21q22 rearrangements; actually, they may also be found after alkylating agents treatment and/or radiotherapy; the prior cancer is variable: breast cancer, non-Hodgkin lymphoma, Hodgkin disease, leukaemia, lung carcinoma, and other malignancies.

up to 30% of t(11;19)(q23;p13.1), 10% or more of t(9;11), 5% of t(4;11) and 5% of t(10;11) are found in secondary leukaemias: altogether 5 to 10% of 11q23 leukaemias are treatment related; these 11q23 second leukaemias are found at any age, from infancy to elder age.

latency for the outcome of the second leukaemia after the first cancer is often short (med 2 yrs), but highly variable, and may not depend on the type of treatment received; it is however most often shorter than in cases of second leukaemias associated with -5/del(5q) or with -7/del(7q).

is poor, as in other therapy related leukaemias; in a recent excellent studyc (n=40), only 80% of patients achieved remission, 3/4 relapsed within a year; median remission duration being 5 mths.

various 11q23 rearrangements may be found:- t(1;11)(p32;q23)- t(1;11)(q21;q23)- t(4;11)(q21;q23)- t(6;11)(q27;q23)- t(9;11)(p22;q23)- t(10;11)(p12;q23)- t(11;16)(q23;p13)- t(11;17)(q23;q25)- t(11;19)(q23;p13.3)- t(11;19)(q23;p13.1)

del(6q), -7/del(7q), del(17p)

5 MLL - 3 partnerN-term AT hook and DNA methyltransferase from MLL fused to (little or most of) the partner C-term part.

11q23 rearrangements are also -and more often- found in de novo leukaemia